Heat Shock Protein 22 Attenuates Doxorubicin-Induced Cardiotoxicity via Regulating Inflammation and Apoptosis
出版年份 2020 全文链接
标题
Heat Shock Protein 22 Attenuates Doxorubicin-Induced Cardiotoxicity via Regulating Inflammation and Apoptosis
作者
关键词
-
出版物
Frontiers in Pharmacology
Volume 11, Issue -, Pages -
出版商
Frontiers Media SA
发表日期
2020-03-25
DOI
10.3389/fphar.2020.00257
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Management of cardiovascular risk in patients with multiple myeloma
- (2019) Chris Plummer et al. Blood Cancer Journal
- Tat-HSP22 inhibits oxidative stress-induced hippocampal neuronal cell death by regulation of the mitochondrial pathway
- (2017) Hyo Sang Jo et al. Molecular Brain
- NLRP3 Deficiency Reduces Macrophage Interleukin-10 Production and Enhances the Susceptibility to Doxorubicin-induced Cardiotoxicity
- (2016) Motoi Kobayashi et al. Scientific Reports
- Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation
- (2016) Lin-Lin Kang et al. Scientific Reports
- Novel Role for Caspase-Activated DNase in the Regulation of Pathological Cardiac Hypertrophy
- (2015) L. Gao et al. HYPERTENSION
- Renalase is a novel target gene of hypoxia-inducible factor-1 in protection against cardiac ischaemia–reperfusion injury
- (2014) Meng Du et al. CARDIOVASCULAR RESEARCH
- The valosin-containing protein promotes cardiac survival through the inducible isoform of nitric oxide synthase
- (2013) Paulo Lizano et al. CARDIOVASCULAR RESEARCH
- Role of HMGB1 in doxorubicin-induced myocardial apoptosis and its regulation pathway
- (2012) Yongwei Yao et al. BASIC RESEARCH IN CARDIOLOGY
- Doxorubicin-induced cardiomyopathy: From molecular mechanisms to therapeutic strategies
- (2012) Yanti Octavia et al. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
- Anandamide enhances expression of heat shock protein 72 to protect against ischemia–reperfusion injury in rat heart
- (2012) Qian Li et al. Journal of Physiological Sciences
- Preemptive conditioning of the swine heart by H11 kinase/Hsp22 provides cardiac protection through inducible nitric oxide synthase
- (2011) Li Chen et al. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
- Novel Toll-like receptor-4 deficiency attenuates trastuzumab (Herceptin) induced cardiac injury in mice
- (2011) Nasser Ghaly Yousif et al. BMC Cardiovascular Disorders
- Small Heat Shock Proteins Induce a Cerebral Inflammatory Reaction
- (2011) I. B. Bruinsma et al. JOURNAL OF NEUROSCIENCE
- Flavaglines Alleviate Doxorubicin Cardiotoxicity: Implication of Hsp27
- (2011) Yohann Bernard et al. PLoS One
- Akt mediates 17β-estradiol and/or estrogen receptor-α inhibition of LPS-induced tumor necresis factor-α expression and myocardial cell apoptosis by suppressing the JNK1/2-NFκB pathway
- (2010) Chung-Jung Liu et al. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
- Cardiovascular Complications of Cancer Therapy
- (2009) Edward T.H. Yeh et al. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
- Roles of ERK and NF-κB in Interleukin-8 Expression in Response to Heat Shock Protein 22 in Vascular Smooth Muscle Cells
- (2009) Seung-Hun Kang et al. KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Shared Principles in NF-κB Signaling
- (2008) Matthew S. Hayden et al. CELL
- Heat Shock Protein 20 Interacting With Phosphorylated Akt Reduces Doxorubicin-Triggered Oxidative Stress and Cardiotoxicity
- (2008) Guo-Chang Fan et al. CIRCULATION RESEARCH
- Toll-like receptor-4 deficiency attenuates doxorubicin-induced cardiomyopathy in mice
- (2008) Alexander Riad et al. EUROPEAN JOURNAL OF HEART FAILURE
- Structure, properties, and functions of the human small heat-shock protein HSP22 (HspB8, H11, E2IG1): A critical review
- (2007) Anton A. Shemetov et al. JOURNAL OF NEUROSCIENCE RESEARCH
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationCreate your own webinar
Interested in hosting your own webinar? Check the schedule and propose your idea to the Peeref Content Team.
Create Now